Dental research has developed substantial evidence that dental plaque is the predominant etiological factor responsible for both periodontal disease and dental caries. Dental caries is the localized, progressive decay of the teeth. It results from tooth demineralization brought about by acids formed when bacteria in dental plaque ferment carbohydrate foods present in the mouth.
Dental plaque is a deposit which accumulates on the teeth and adjacent surfaces in the oral cavity. The plaque is a product of microbial growth, primarily derived from food residues in the mouth. Mucoproteins and minerals present from the saliva and dead cells in the mouth also assist in plaque formation.
Plaque is removed to some extent by effective brushing of the teeth, but the less accessible and more sheltered areas of the mouth which cannot be readily reached by a toothbrush, are particularly susceptible to plaque and eventual calculus growth. Left unhindered, the plaque increases in size and more tenaciously adheres to the teeth. The bacterial metabolism within the plaque on the tooth surface results in the production of acids, toxins and enzymes which are deleterious to the neighboring oral tissues. There is evidence pointing to plaque as being the direct cause of dental caries, due to the generation of acids within the plaque structure.
To protect a normal tooth, a thin layer of dental enamel forms a protective coating over the tooth. This coating consists mainly of calcium, phosphate, and other ions in a hydroxyapatite-like structure. The enamel contains 2-5 percent carbonate, which makes the enamel susceptible to acid dissolution.
The interaction of three factors is believed to result in dental caries: a susceptible tooth surface; microflora; and suitable substrate for the microflora. Although several acidogenic microorganisms that are present in the mouth can initiate carious lesions, Streptococcus mutans is believed to be the primary pathogen.
It is known that foods containing fermentable carbohydrates can promote dental caries. Tooth decay begins when the Streptococcus mutans, that reside principally in the plaque that adheres to a tooth surface, metabolize the fermentable carbohydrates consumed by the host. During the metabolism of the fermentable carbohydrates by the bacteria, lactic acid and other organic acids are secreted as a by-product. These acids reduce the pH of the surrounding plaque/tooth environment.
When the pH of the plaque/tooth environment drops below a critical level of 5.5 to 5.7, hydroxyapatite (calcium phosphate hydroxide, Ca.sub.10 (PO.sub.4).sub.6 (OH).sub.2), the key component of tooth enamel, begins to dissolve. Typically, the dissolution begins below the tooth's porous surface.
With repeated acid attacks, caused by the further metabolism of fermentable carbohydrates by the bacteria, subsurface lesions expand. If the lesions expand to the point that the enamel surface breaks, a cavity is formed and the process is no longer reversible.
The natural remineralization process involves, in part, the flow of saliva over the plaque. The saliva can raise the pH of the environment. Additionally, calcium and phosphate ions in the saliva precipitate out to replace the hydroxyapatite that was dissolved by the organic acids created during the metabolism of the fermentable carbohydrates.
Typically, this remineralization process only occurs at significant levels when the pH is above the critical level. If the saliva does not sufficiently raise the pH, significant remineralization will not occur. The remineralization process may be enhanced by fluoride in the oral cavity that speeds up new crystal growth and makes a fluorapatite-like material that is precipitated on the surface of the crystals inside the carie lesion.
The most important single factor contributing to periodontal disease is the accumulation of plaque and dental calculus (e.g., salivary tartar) on the teeth. These deposits result in tissue inflammation of the surrounding gingiva, and, as the condition increases in severity, the supporting bone is also affected. These reactions lead to the destruction of the supporting structures and the subsequent mass loss of teeth which are usually free of decay.
Although brushing the teeth with a toothbrush and dentifrice is a widely recognized technique for maintaining dental health, the average American brushes only about once a day for approximately one minute. Therefore, a great need exists for finding additional methods for improving daily oral hygiene. Chewing gum has over the years been advocated as a possible excellent adjunct for cleaning the teeth, because people find chewing of gum very pleasurable and chew gum for much longer periods of time than they brush their teeth. Chewing gum is especially advantageous for use in circumstances where toothbrushing is not possible or convenient, such as after lunch, while traveling, or while working.
In general, chewing gum comprises a neutral and tasteless masticatory chewing gum base and one or more non-masticatory active ingredients mixed into the base. As used herein, an "active ingredient" is an ingredient such as a sweetener; a flavoring agent which determines flavor and taste characteristics of the gum; a body-treating ingredient such as a medicinal drug or pharmaceutical agent which is released at a gradual rate and ingested during chewing; or a breath-freshening ingredient which treats or reduces oral malodor. In addition, the chewing gum may contain water-soluble and usually sweet non-masticatory bulking agents, a coloring agent, or a plasticizing agent which is employed to improve the texture of the gum.
Certain active chewing gum ingredients benefit from or require encapsulation in order to achieve a gradual and controlled release of the ingredients during chewing or to promote their stability in chewing gum.
U.S. Pat. No. 5,139,794 describes a chewing gum which has a content of an encapsulated sodium chloride ingredient. The coating on the sodium chloride particles provides a prolonged flavor-enhancing effect without imparting a salty taste.
Of background interest with respect to the present invention are publications which disclose chewing gum products containing a bicarbonate salt such as sodium bicarbonate. Prior art references include U.S. Pat. Nos. 4,148,872; 4,150,112, 4,156,715; 4,156,716; 4,157,385; 4,159,315; 4,160,054; 4,160,820; 4,170,633; 4,269,860; 4,639,368; 4,867,989; 4,952,407; 4,997,667; 5,077,051; and the like.
There is continuing interest in the development of novel chewing gum products which provide dental health benefits during normal usage.
Accordingly, it is an object of this invention to provide a chewing gum product which can serve as a convenient adjunct for improved dental health.
It is another object of this invention to provide a chewing gum product which has a content of encapsulated therapeutic ingredient for oral hygiene which is sustain-released over a prolonged period under oral chewing conditions.
It is another object of this invention to provide a chewing gum product which counteracts bacteria-generated acids, enhances saliva flow, and exhibits plaque-inhibiting activity.
It is a further object of this invention to provide a chewing gum product with a content of encapsulated flavorant ingredient which has a prolonged taste effect under oral chewing conditions.
Other objects and advantages of the present invention shall become apparent from the accompanying description and examples.